scholarly journals Pathology of oral squamous cell carcinoma. Morphological evaluation of cancer cell nests, patterns of invasion and grading of malignancy.

1999 ◽  
Vol 11 (4) ◽  
pp. 379-385
Author(s):  
Takao Kohgo
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cancer Cell ◽  
Squamous Cell ◽  
Morphological Evaluation

Erianin Induces Apoptosis and Autophagy in Oral Squamous Cell Carcinoma Cells

2020 ◽  
Vol 48 (01) ◽  
pp. 183-200 ◽  
Author(s):  
Yi-Tzu Chen ◽  
Ming-Ju Hsieh ◽  
Pei-Ni Chen ◽  
Chia-Jui Weng ◽  
Shun-Fa Yang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Cancer ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cancer Cell ◽  
Squamous Cell ◽  
Mapk Signaling ◽  
Therapeutic Interventions ◽  
Oral Cancer Cell ◽  
Close Relationship

Oral squamous cell carcinoma (OSCC) is a leading cause of cancer-related deaths worldwide. It has a very poor prognosis with over a 5-year survival rate of only 50%. Thus, it is important to identify effective therapeutic interventions against oral cancer. Apoptosis and autophagy have reported genetically regulated in physiology and diseases, which close relationship. Many natural compound study objects anticancer effect have been studied between apoptosis and autophagy relationship. The present study was designed to evaluate the effect of erianin on human oral cancer cell proliferation. Results of the study revealed that treatment with erianin significantly reduced the viability of different OSCC cell lines. Erianin exerted its cytotoxic effect by inducing cell cycle arrest and caspase-dependent apoptotic pathways. Both intrinsic and extrinsic pathways were found to be involved in erianin-mediated cell death. In addition, treatment with erianin also increased autophagy in OSCC cells. With further analysis, it was found that erianin induced both apoptosis and autophagy by regulating MAPK signaling pathways. Taken together, our study indicates that erianin plays an important role in reducing oral cancer cell viability, and thus, can be considered as a potential anticancer agent.

scholarly journals High level of calpain1 promotes cancer cell invasion and migration in oral squamous cell carcinoma

2017 ◽  
Vol 13 (6) ◽  
pp. 4017-4026 ◽  
Author(s):  
Da Ma ◽  
Juan Fang ◽  
Ying Liu ◽  
Jing-Jing Song ◽  
Yan-Qiong Wang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cancer Cell ◽  
Squamous Cell ◽  
Cell Invasion ◽  
Cancer Cell Invasion ◽  
Invasion And Migration ◽  
And Migration ◽  
High Level

scholarly journals The Crossroads of Periodontitis and Oral Squamous Cell Carcinoma: Immune Implications and Tumor Promoting Capacities

2021 ◽  
Vol 1 ◽  
Author(s):  
Omnia Elebyary ◽  
Abdelahhad Barbour ◽  
Noah Fine ◽  
Howard C. Tenenbaum ◽  
Michael Glogauer
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cancer Cell ◽  
Cancer Progression ◽  
Squamous Cell ◽  
Immune Escape ◽  
Inflammatory Responses ◽  
Gingival Tissue ◽  
Local Inflammatory Response

Periodontitis (PD) is increasingly considered to interact with and promote a number of inflammatory diseases, including cancer. In the case of oral squamous cell carcinoma (OSCC) the local inflammatory response associated with PD is capable of triggering altered cellular events that can promote cancer cell invasion and proliferation of existing primary oral carcinomas as well as supporting the seeding of metastatic tumor cells into the gingival tissue giving rise to secondary tumors. Both the immune and stromal components of the periodontium exhibit phenotypic alterations and functional differences during PD that result in a microenvironment that favors cancer progression. The inflammatory milieu in PD is ideal for cancer cell seeding, migration, proliferation and immune escape. Understanding the interactions governing this attenuated anti-tumor immune response is vital to unveil unexplored preventive or therapeutic possibilities. Here we review the many commonalities between the oral-inflammatory microenvironment in PD and oral-inflammatory responses that are associated with OSCC progression, and how these conditions can act to promote and sustain the hallmarks of cancer.

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